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Pulmonary SP-A: Forms and Functions

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Animal Lectins: Form, Function and Clinical Applications

Abstract

Pulmonary surfactant is a complex mixture of lipids and proteins, and is synthesized and secreted by alveolar type II epithelial cells and bronchiolar Clara cells. It acts to keep alveoli from collapsing during the expiratory phase of the respiratory cycle. After its secretion, lung surfactant forms a lattice structure on the alveolar surface, known as tubular myelin. Surfactant proteins (SP)-A, B, C and D make up to 10% of the total surfactant. SP-B and SPC are relatively small hydrophobic proteins, and are involved in the reduction of surface-tension at the air-liquid interface. SP-A and SP-D, on the other hand, are large oligomeric, hydrophilic proteins that belong to the collagenous Ca2+- dependent C-type lectin family (known as “Collectins”), and play an important role in host defense and in the recycling and transport of lung surfactant. There is increasing evidence that surfactant-associated proteins A and -D (SP-A and SP-D, respectively) contribute to the host defense against inhaled microorganisms. Based on their ability to recognize pathogens and to regulate the host defense, SP-A and SP-D have been recently categorized as “Secretory Pathogen Recognition Receptors”. In nut-shell, the four lung-specific surfactant-associated proteins: SP-A, SP-B, SP-C, and SP-D serve a number of different roles, including enhancement of surface-active properties of surfactant glycerophospholipids, surfactant phospholipid reutilization, and immune defense within the alveolus. Surfactant proteins, SP-A and SP-D contribute significantly to surfactant homeostasis and pulmonary immunity. Their basic structures include a triple-helical collagen region and a C-terminal homotrimeric lectin or CRD. The trimeric CRDs can recognize carbohydrate or charge patterns on microbes, allergens and dying cells, while the collagen region can interact with receptor molecules present on a variety of immune cells in order to initiate clearance mechanisms. Gene knock-out mice models of lung hypersensitivity and infection, and functional characterization of cell surface receptors have revealed the diverse roles of SP-A and SP-D in control of lung inflammation (Kishore et al. 2006)

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  1. Department of Biomedical Engineering, Rayat and Bahra Institute of Engineering and Biotechnology, Kharar (Mohali), Punjab, India

    Anita Gupta (Assistant Professor)

  2. Vaccine Production Division, Panacea Biotec, Lalru (Mohali), Punjab, India

    Rajesh K. Gupta (General Manager)

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Gupta, A., Gupta, R.K. (2012). Pulmonary SP-A: Forms and Functions. In: Animal Lectins: Form, Function and Clinical Applications. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1065-2_24

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